Vertical Divider

Above, field workers in a prairie dog colony that was extirpated in the previous year.

Strong selection such as that exerted by introduced pathogens should, in the presence of genetic variation, elicit adaptation.  Indeed, rapid adaptation has been observed in response to numerous anthropogenic stressors.  But in many cases, adaptation is ephemeral or spatially localized, hinting at constraints.  We are using plague resistance in prairie dogs to test for constraints imposed by the landscape (e.g., dilution of adaptive alleles), by genomes themselves (e.g., epistasis), and by ecological or demographic stochasticity (e.g., resistant prairie dogs experience amplified predation in nearly-extirpated populations).

Prairie dog populations are threatened by the compounded effects of habitat fragmentation and sylvatic plague, caused by the non-native bacterium Yersinia pestis, which was introduced to North America in the early 1900s.  Plague is highly virulent to prairie dogs, and epizootics eliminate entire colonies.  Beginning in the late 1990s, however, survivors of these epizootics have been detected in two species -- Gunnison's and black-tailed prairie dogs -- in at least three states.

Our collaborators have showed that resistance is higher in black-tailed prairie dog populations that have the longest coevolutionary history with Yersinia pestis, supporting the idea that resistance is evolving.  The presence of genetic variation for resistance, the relatively high mobility of prairie dogs, and the strength of selection from the pathogen suggest that resistance should be widespread.  Yet most populations are still highly susceptible to the pathogen, continuing to experience extirpations during epizootics.  This observation indicates there are likely constraints to resistance, and we seek to understand those constraints.

Vertical Divider

In 2007, a plague epizootic began in Boulder County, Colorado. Out of the hundreds of prairie dogs we captured before, during, and after the epizootic, we detected 7 that survived plague.  A genome-wide association test revealed several loci (including those on the scaffold pictured at left) that were associated with survival from plague. 

Some of these loci are related to T-cell function, and one (ICOS) was implicated in survivorship from the Black Death in humans! (Klunk et al. 2022)

Plague extinctions and recolonization also influence genetic diversity at the scale of individual prairie dogs:  Prairie dogs in populations that had been recolonized had significantly higher heterozygosity than prairie dogs in those populations before plague (left figure, below).  Moreover, heterozygosity of six survivors (vertical bar in right figure, below) was strikingly higher than expected due to chance.  This work contributes to our understanding of how animals evolve in response to introduced diseases, especially in anthropogenically altered landscapes.  This work was funded primarily by the Boulder County Nature Association, the University of Colorado Natural History Museum, the University of Colorado (CU) and CU’s Department of Ecology and Evolutionary Biology.  You can read the full paper here and find out about my ongoing work--which seeks to explore the genetic underpinnings of resistance and why resistance is not more widespread--here.

Reference:  L.C. Sackett, S.K. Collinge, A.P. Martin 2013.  Do pathogens reduce genetic diversity of their hosts?  Variable effects of sylvatic plague in black-tailed prairie dogs.  Molecular Ecology 22: 2441-2555.  Download PDF


Collaborators:

Andy Martin, University of Colorado
Ryan Jones, University of Arizona
Sharon Collinge, University of Colorado